Colorectal cancer (CRC) is the second most common malignancy in women and the third most common malignancy in men worldwide (1). Although CRC mortality has been declining due to improvements in screening techniques and CRC treatment, it is still the second most common cause of cancer-related death. Therapeutic approaches for CRC have included antimetabolite drugs interfering in biosynthetic processes. However, these compounds do not specifically target cancer cells alone, resulting in a number of side-effects. More specific targeted therapies have also been used. In particular, inhibitors of the Epidermal Growth Factor Receptor (EGFR) have been used (2-4). EGFR is a kinase, whose activity results in phosphorylation and activation of downstream signaling cascades such as the Ras-Raf-MEK-ERK and PI3K-PKB/Akt pathways (5). However, some CRCs harbor an activating mutation in the Ras gene (6), rendering the use of upstream EGFR inhibitors ineffective (7). Pan-kinase inhibitors (e.g. Regorafenib (8)) or selective kinase inhibitors (e.g. PI3K/AKT inhibitors (9)) are currently being tested, however, the potential for side effects is present as phosphorylation of proteins and lipids is essential for virtually all cellular functions. While kinases have so far been targeted for treatment, phosphatases are generally regarded as tumor suppressors and have for the most part been disregarded in cancer research.